title: Simulating the role of anisotropy in human atrial cardioversion.
abstract: This computational study quantifies the effectiveness of feedback controlled low energy cardioversion in the anisotropic human atria. An established biophysical human cell model was adopted to reproduce Control and chronic atrial fibrillation (CAF) action potentials. The cell model was combined with a detailed human atrial geometry to construct a 3D realistic human atrial model. Scroll waves were simulated under Control and CAF conditions and the cardioversion parameters of stimulation strength and pacing duration were evaluated for scroll wave termination. Scroll waves were initiated at two locations in the atria to elicit the effects of scroll wave location. The role of anisotropy was highlighted by comparison to results from the isotropic case. Under Control conditions, scroll wave self-termination was rapid in the anisotropic case. Under CAF conditions, anisotropy caused the initiated scroll wave to degenerate into multiple scrolls with each evolving erratically or pinning to anatomical defects. The cardioversion successfully terminated scroll waves within 10 s, but the stimulus strength had a strong correlation to the location of the scroll wave. The low energy stimulation strength was always lower than the threshold stimulus. Anisotropy plays an important role in atrial electrical properties. Anisotropy aggravates CAF and leads to high frequency atrial pacing. The efficacy of cardioversion is significantly affected by anisotropy.
authors.forename: Sanjay R
authors.initials: SR
authors.lastname: Kharche
authors.forename: Irina V
authors.initials: IV
authors.lastname: Biktasheva
authors.forename: Henggui
authors.initials: H
authors.lastname: Zhang
authors.forename: Vadim N
authors.initials: VN
authors.lastname: Biktashev
mesh_terms: D000200:Action Potentials / Q000502:physiology; D016880:Anisotropy; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy; D004554:Electric Countershock; D006325:Heart Atria / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular